Thursday, March 19, 2009

Rats Prevent Plague?

Like so much that is fundamental to history (Whatever happened to the Dust Bowl? Why did the Japanese bomb Pearl Harbor?), this question is sidestepped by most grade-school teachers.

The simple truth is that RATS ended Bubonic Plague pandemics in Europe -- an odd but true story that, no doubt has been suppressed by public health officials uncomfortable with such inconvenient truths.First, a little history. Plague has probably swept through the Old World time and time again. Plague-like pestilences are mentioned in the Bible (the so-called “scourge of the Philistines”), and at least five great outbreaks are noted by historians.

For modern purposes, however, the "big plague" was the so-called "Black Death" that swept through Europe beginning in the 14th Century and carried forward, with fits and starts, until the middle of the 17th Century.

The first wave of this plague killed off one-third of the population of Europe within two years of its arrival in the port of Messina, Sicily in 1346.

The vector, or transmission agent, for this wave of Bubonic Plague was the black rat Ratusratus, which was host to the black rat flea, Xenopsyllacheopis, which in turn was host to the bacterium Yersiniapestis that actually causes the Plague.

Large-scale incidents of plague in Europe ended with the arrival of a very aggressive new immigrant -- Ratusnorvegicus, aka the Brown or "Norwegian" rat.

In fact this rat is not Norwegian. It probably originated in Asia, and got to Europe through the Middle East, first arriving in England on a load of timber from Norway (hence the name given to it by the British)The Brown Rat and the Black Rat look somewhat similar, but they have very different temperaments.

A Brown Rat is not only larger that its Black Rat cousin, it is also far more aggressive. When the Brown Rat arrived in Europe and began to multiply, it quickly pushed the smaller and more mouse-like Black Rat out of buildings, alleys, storage sheds and sewers. In fact, over time, it pushed the Black Rat almost totally out of existence in the temperate world.

Though fleas and lice are opportunists, they tend to gravitate towards, and specialize in, certain hosts. Different species of bird lice, for example, specialize in different species of birds. In fact, many species of bird lice can only be found on very specific bird species. The extinction of a bird species may, in turn, result in the extinction of one or more species-specific types of bird lice.

Many types of flea also gravitate towards, and special in, certain kinds of hosts. Though a species of flea may theoretically be able to draw a blood meal from a wide variety of mammalian hosts, most thrive on a specific list of hosts and generally fail to thrive if these particular hosts are not around.

So it is with Xenopsyllacheopis, the oriental rat flea, which is the flea most likely to be implicated in transmission of the Bubonic Plague.

The oriental rat flea thrives on a few species of rodents, and the Black Rat is far and away the most common of its rodent-host carriers.

With the rapid spread of the Brown Rat in Europe, the Black Rat was bullied and beaten into extirpation across most of the civilized world.

Today the Black Rat is commonly found only in the tropics. Even there it is most likely to be found high up (running along roofs and feeding at the tops of date palms) in order to avoid running into the neighborhood bully, the Brown Rat.

Bottom line: the Bubonic Plague was brought to Europe by fleas riding on Black Rats, while Brown Rats largely drove that species of rat out of Europe (and much of the rest of the world), thus eliminating the oriental rat flea and the Yersiniapestis bacteria that brought with it the Bubonic Plague.

The Black Death was not bubonic plague at all, but was in fact a now-unknown viral haemorragic agent, with an infectious incubation period of a couple of weeks or so.

In medieval Britain, at the time of the Black Death outbreaks, the only rats present were in the ports; there were absolutely no rats of any description in the bulk of the countryside. You can see that from architecture of dovecots; there is no attempt made to keep the nesting doves away from rats. You can also see it in owl pellets excavated from medieval layers; modern owls are very capable rat killers and the pellets they produce always contain rat bones. Owl pellets from medieval, pre-Rattus norvegicus layers don't contain rat bones except in port towns, where Rattus rattus didn't breed (it was at the very northernmost extreme of its range even then, in the warm medieval times) but where the population was continually topped up from ship rats.

Medieval people were highly superstitious and regarded unusual events as Acts of God. Bubonic plague, when it occurs, is a zoonotic disease; it is primarily a disease of rodents which can also affect people, and in an outbreak the first things hit are the rats. This creates massed panic in the rat population, followed by a mass die-off featuring rats lying dead everywhere. Only when the rodent hosts are mostly dead do the starved fleas try biting humans and spread plague to the human population.

So, had the Black Death been bubonic plague, you would have had reports of God producing a plague of diseased rats which then spread plague to the people of a town. Needless to say, there are no such reports.

The Black Death also doesn't behave epidemiologically like a rat-vectored disease; it seemed to spread at the same rate in rural, spread-out populations as it did in densely-populated cities, leading to the conclusion that it was a human-to-human spreading disease, not a rat-vectored one.

Finally, there is the genetic evidence. In mammal immune systems any foreign antigen is presented to immune cells in the lymph nodes by attaching it to the surface of the Major Histocompatibility Complex molecules; a sort of molecular level silver platter to present an unknown object upon. MHC molecules vary a lot. Some are best adapted to presenting antigens of viral origin, some of bacterial origin, some of parasitic origin. African peoples have MHC molecules biased towards bacterial and parasitic antigens, though their spread can really be called generalist.

European peoples have MHC molecules strongly biased towards viral antigens, this being the genetic relic of a viral plague which selectively killed off people whose immune systems were not quite so good at handling viruses as were most people. The only large-scale plagues which are known to have occurred recently enough to show this effect are the Black Death plagues, which again argues against the disease being bacterial (i.e. bubonic plague) and for it being a virus of some sort.

In conclusion, you are wrong regarding bubonic plague being the source of the Black Death. Nice pictures, though.

Trivia: A friend of mine is the zookeeper in charge of the Black Footed Ferrets at our zoo. BF Ferrets are very endangered, in large part because their main diet is Prairie Dogs, and Prairie Dog populations are infected with the Plague.

Sorry Dan Holdworth, but typing does not pass for research or knowledge on this blog, and what you have written is documentable nonsense.

In fact, rats were all over Europe (England too), and the Plague was hardly confined to England was it?

As to the notion that the Plague was not the Plague, but was Viral Hemorrhagic Fever, that matter has been layed squarely to rest by excavations of the Plague dead and tests on tooth pulp which show (suprise!) that the Bubonic Plague was the cause of the Black Death.

This is not closely held information. See >> http://www.pnas.org/content/95/21/12637.full or any of the other papers on other plague-era excavations written about since.

I always find it astounding that people would write 7-8 paragraphs without taking the time to do a simple Google search.

As you so rightly point out, a little googling of sources is quite a good idea. Reading the following (which was linked from the paper you cited) might prove illuminating: http://mic.sgmjournals.org/cgi/content/abstract/150/2/341

Excavating plague dead is always fraught with difficulty since as you are no doubt aware a haemorragic virus would use RNA as its nucleic acid, which is much less persistent than is DNA, hence not finding nucleic acids from a haemorragic virus is hardly good evidence of absence. Furthermore detecting Yersina pestis in a minority of samples is again not particularly good evidence of it being the plague agent; nobody is denying that Y. pestis was present in the medieval environment, only that it wasn't the major infective agent.

Similarly the following review summarises my main points quite nicely: http://pmj.bmj.com/cgi/content/full/81/955/315 and argues quite convincingly that Y. pestis was not the major cause of the Black Death.

The conclusion here is obvious even to the most foolish reader: bubonic plague was not the Black Death, but an unknown haemorragic virus with a long infectious incubation period was the causitive agent, and surveillance and disease control strategies need to be concentrated upon this organism, not on the admittedly nasty but ultimately blameless Y. pestis organism. It would also be a really good idea to try to find the Black Death virus so a vaccine can be developed, before it re-appears again.

Well, Googling is good but I suppose I should also add that a little knowledge is a dangerous thing, LOL.

Not too surprisingly you point to the discredited work of Duncan andScott, the originators of a thesis they invented whole cloth.

The core of their thesis is that the plague was caused by a mysterious unnamed disease.

What was it? They are not sure.

Do they have evidence that it was not the plague? No they do not.

Instead, Duncan and Scott assemble a lot of circumstantial bits andpieces similar to the folks who write books saying that Martians built the pyramids and that the CIA created HIV to kill black people in Africa. Too bad their thesis has rather quickly crashed on the rocks of reality and polymerase chain reaction.

First, and just for fun, let's ask who Susan Scott and Christopher J.Duncan are. Well for one thing, neither one of them areepidemiologists. Scott is a "research worker in historical demography" at the University of Liverpool, while Duncan is a professor of zoology at the same school.

There is nothing wrong with either of these two fields -- I have anadvanced degree in demographics myself (Georgetown University), and know a bit about animals as well (I used to be Director of the Population and Habitat Program at the National Audubon Society), but I do think that necessarily qualifies me to write about zoonotic epidemics. Generally,when we want to know about epidemics, we go to ....wait for it ...an epidemiologist.

The good news for readers of this blog is that Tara Smith, anepidemiologist at the University of Iowa and the deputy director of the University of Iowa Center for Emerging Infectious Diseases, has an excellent summary of the debate on her epidemiological blog.

For those who want to cut to the chase, Smith notes that Duncan andScott are "rather selective in what evidence they choose" and thatDuncan and Scott embrace any and all evidence that supports their thesis while ignoring all evidence that does not.

Smith notes that in many cases Duncan and Scott make bold assertions without any evidence at all, and that they engage in circular logic to bolster their thesis.

Most damaging of all, Smith notes the mysterious disease they describe "is consistent with bubonic plague," while -- laughably -- Scott andDuncan cite the work of Daniel Defoe (yes the fiction writer), writing in 1722 as being that of an eye witness observer of a plague that occurred in 1665! Ouch. Talk about embarrassing "research"!

Tara Smith nicely summarizes this tempest in a teapot:_ _ _ _

"I think it's been pretty well established, using both historicalepidemiology as well as paleomicrobiological methods, that Y. pestis[aka the Bubonic Plague] was the cause of the Black Death and otherplague outbreaks that occurred both before and after the mid 14thcentury. This doesn't rule out the occasional misdiagnosis, or localizedoutbreak caused by a different pathogen, but the bulk of the evidencepoints to Y. pestis as the culprit."

But wait....According to Tim Severin, in his book, In Search of Genghis Khan, the original reservoir of the bubonic plague and still able to pass it directly to humans today, is....marmots, which live, or lived, all across the steppe in Central Asia.

"Plague bacillus was extraordinarily resilient...known to survive in dried human sputum for as long as three months....the carriers that spread the disease could be animals, but equally they could be infected humans or the fleas themselves..."

"Marmot sickness", as the Mongols themselves called it, was reported by Rubruck, who was in Mongolia a generation after Genghis Khan, which would have been around 1300.

"It is likely that it was the Mongol armies and the merchants who traveled under Mongol protection who brought the most lethal version of the disease to the West."

To this day, in Mongolia, marmot hunting is immediately suspended when plague appears. The arats, or herders, know that a normal marmot is alert and curious. A hunter waves a small white flag to get the marmot to stand upright, so it can be shot. If the animal shows signs of drowsiness or lack of alertness, that would be,uh, a red flag. Likewise, sick and dying marmots was a signal to stay away from that area.

The marmots harbor a more virulent form of the disease than other animals like rats and feral dogs.

By the way, many Mongols love, love, love marmot. They roast it with hot rocks in the chest cavity after removing the fur with a blowtorch.

My Source: Severin spoke with the Minister of Public Health in Ulaanbaatar in about 1991.

Great book, highly recommended. I just did a review of it on my blog. Severin does REALLY serious adventure travel.

Foxstudio -- See the links at the end of this post entitled "Tarvag for Dinner Again?" , and "Where did Bubonic Plague Go? "

Tarvag is the marmot of mongolia and a national dish.

For the record, the black rat flea (or Tarvag flea if you prefer) needs a DRY environment as well as a specific host, which is why the only true sinks for the disease are in China, and the North American west (prairie dog towns), and south American deserts. The last two locations are places infected after 1900, as I note in the links.

I'm afraid that my take on this has now completely reversed; I now completely agree with Mr Burns on the subject of what caused the Black Death (Yersina pestis) and furthermore think that the unknown virus theory is bunk.

The reason is this: the major plank of the unknown virus theory is that Rattus rattus is absolutely needed as a reservoir host for plague. This notion is completely false; plague bacillus is not especially choosy about its hosts, and will infect most rodents, domestic cats and humans.

Plague certainly got into Britain in black rats, but it didn't need them as a reservoir host and could quite happily have ticked over in native rodents and been periodically retransmitted to human settlements by these rodents, or by cat fleas (which are gloriously non-specific feeders and readily bite people as well as cats).

This removes the major argument in favour of the unknown virus and leaves that theory with another major problem: where did a virus that is obviously very strongly adapted to humans come from, and why did it die out after several centuries happily circulating in rural France? Things like this don't easily die out (think of the trouble we had exterminating smallpox) and it should still be out there somewhere.

No, I'm afraid my previous argument was spurious bunk and completely false. I am now in complete agreement with Mr Burns on this one.

Pai, I would describe the notion that there is a causal link between the Plague and HIV resistance as speculative and not all that well founded.

To start with, how do we know who is the descendent of someone who survived the Plague? Most of us cannot name our great, great grandfathers, and the 1300's were a long time ago!

A lot of people survived the plague in Europe for a simple reason unrelated to genetics -- they were lucky and did not get bitten by a flea and were not coughed on by a sick neighbor.

That said, there is a gene -- CCR5 -- which seems to confer some benefits on both counts (plague and HIV), but the idea that mutation was *caused* by the plague is clearly wrong. Mutation is caused by mutation, and a gene survives (or fails to replicate) based on whether it confers a benefit of some sort.

The CCR5 gene most commonly occurs among nordic people where the plague has the hardest time gaining hold due to weather. If it was a gene that benefited plague victims a lot, you would expect it to be most prevalent in Mongolia where the plague originated and is still pretty common, but apparently that is not the case. Apparently the gene did not pop up where it was MOST needed -- it popped up where it was LEAST needed.

More likely CCR5 is simply an odd and spontaneous gene mutation that predates the Plague and HIV, which makes it hard for very old diseases of several types to lock in -- a benefit for a lot of diseases, not just the plague and HIV. It is famously true that Norwegians live forever. The CCR5 gene might help explain why.

A medicine that tries to artificially replicate CCR5 benefits has been greenlighted. We will see if much comes from it. Since we do not know what the CCR5 gene does (many genes do several things) we are not too sure what happens when we start playing with it.

The Plague, for the record, is a simple bacteria, well undersood, and pretty easily treatable with antibiotics. HIV is a retroviral disease, and quite different, which is why it has stymied a race for both a cure and a preventative. We are not even sure what a virus (or retrovirus) is! Is it alive? Mere code? Debate continues, and this is pretty far outside of my knowledge base (though I get a daily HIV research newsletter from the Kaiser Foundation).

For an engaging look at how groups react to massive, sudden trauma, read John Kelly's book about the plague of the mid 1300s in Europe, "The Great Mortality." It is worth the read just for the anecdotal descriptions of human society under stress. Some communities turn on each other. Some communities deepen their interdependence. I'd love to see some science explaining these group behavior choices.

As an Internal Medicine Doctor in The States, I find this fascinating-and I also swallowed (for a Time) the Kool Aid that the Black Death was NOT Yersinia. Duncan and Scott's strongest argument is actually the Rapid Spread of the Disease at a time when people shlepped around on foot or traveled by donkey cart. In the 3rd pandemic at the turn of the last Century, it travelled slowwwlly even as folks got around by locomotive train and steamship. Also, even within Medieval times and the early Renaissance Period, the Black Death NEVER hit as hard as it had in the Mid 14th century. Resistance is commoner with viruses than Bacteria.

I now accept the truth about Black Death but the Brown Rat/Black Rat theory may be erroneous. ALL species of rat and many other rodents, such as the prairie dogs and marmots, and also domestic cats, get Plague and it is rapidly lethal to them. The salient point is that the rat flea does not like to Bite Brown rats. Perhaps they have a natural repellant??